1. SWINE FLU
NEHA SRIVASTAVA
M.PHARM (PHARMACOLOGY)

2. Evolution
1918–19 H1N1 influenza A appeared in pigs, affected 50 million people worldwide
1930 Isolation of H1N1 from pigs for the first time
1970 Transmission of H3N2 virus to swine in Asia
1976 New strain of swine flu variant of H1N1, affected soldiers at Fort Dix in the US
1984 Reassortment between human H3N2 and avian H1N1 in swine

3. 1988 Women exposed to pigs at country fair exhibition in Wisconsin died of H1N1 infection from swine
1994 H1N2, isolated from pigs in the UK. Example of human–avian reassortment
1998 H3N2 virus caused severe disease in North America. Triple reassorted (avian–human–swine) distinct from earlier strains
1958– cases of swine influenza reported among humans
2005–2009 Triple reassortant swine flu virus in human, in United States
2009 New strain of swine influenza H1N1, reported from Mexico and the United States shows sustained human-to-human transmission

4. Swine flu Gene = Swine + Avian + human flu virus
Introduction
Swine Influenza (swine flu) is a-
Respiratory disease of pigs
Type A influenza virus [orthomyxoviridae]
High morbidity and low fatality
Swine flu Gene = Swine + Avian + human flu virus
Scientist call this “Quadruple Re-assortment Virus”.
Incubation : 2-7 days

6. Symptoms

7. Transmission Between pigs.
The direct transfer of the virus probably occurs either by pigs touching noses, or through dried mucus.
Airborne transmission through the aerosols produced by pigs coughing or sneezing
Between humans
Direct transmission
Contact between sick and healthy animals.
Indirect transmission
Feeding with garbage containing infected meat.
Biological vectors: soft ticks of the genus Ornithodoros.
Fomites: premises, vehicles, implements,clothes.

8. MORPHOLOGY OF VIRUS -Hemagglutinin (H) -Neuraminidase (N) Pleomorphic
Two surface antigen-
-Hemagglutinin (H)
-Neuraminidase (N)
Contain 16 hemagglutinin antigen & 9 neuraminidase antigen
8 pieces of segmented negative sense RNA
Matrix protein (M1)-strength & rigidity to envelope
Matrix protein (M2)-target for antiviral
Neuraminidase enzyme that support the virus to cell wall is known as Sialidase

9. Pathogenesis
Step 1- H bind onto sialic acid sugar which is cleaved by protease enzyme and cell import virus
Step 2- Due to acidic endosome viral envelope fuses with vacuole’s membrane and M2 ion channel releases viral RNA & core protein
Step 3- Core protein form complex with viral RNA and transported into nucleus where the RNA-dependent RNA polymerase begins transcribing complementary positive-sense vRNA
Step 4- vRNA either transported to cytoplasm or remain in nucleus
Step 5- Newly synthesised viral proteins are either secreted through the Golgi apparatus onto the cell surface or transported back into the nucleus to bind vRNA and form new viral genome particles. Hemagglutinin and neuraminidase molecules cluster into a bulge in the cell membrane
Step 6- The vRNA and viral core proteins leave the nucleus and enter this membrane protrusion.
Step 7- The mature virus buds off from the cell

10. Different steps of pathogenesis1 2 3 4 5 6 7

11. Diagnosis A) IDENTIFICATION OF THE AGENTS Culture
-cell culture isolation
-egg inoculation test
-haemagglutination test
Swine influenza virus isolates
-haemagglutination inhibition test
-neuraminidase inhibitionn test
Fluorescent test
Polymerase chain reaction test
B) SEROLOGICAL TESTING
Haemagglutination Inhibition test
Enzyme-Linked Immunosorbent Assay

12. Treatment Allopathic Oseltamivir [TAMIFLU] Zanamivir [RELENZA]
Rimantidine [FLUMADINE]
Herbal Therapy
Tulsi
Garlic
Ginger
Gooseberry
Aloe-vera
Camphor

13. Prevention

14. QUERY…. ??